A membrane protein, voltage-dependent Ca2+ channel controls various intracellular actions such as muscular contraction, nerve cell generation and synaptic plasticity, secretion of neutrotransmitter and hormone, and gene expression by regulating calcium ion influx from outside of a cell. As is well known in the art, such voltage-dependent calcium channel is divided into the two main groups based on the requirement voltage for opening channels: high-voltage-activated (HVA) and low-voltage-activated (LVA) Ca2+ channels. Currently, HVA Ca2+ channels are further divided into L-, N-, P/Q-, and R-types and these functional diversities are related to the existence of several α1 subunits (α1A-F and α1s). LVA Ca2+ channels are readily distinguished from HVA Ca2+ channels because they activate at potential near the resting membrane potential and referred to as “transient (T)-type Ca2+ channels” due to their fast inactivation and small conductance. Until recently, three genes encoding T-type Ca2+ channel pore-forming subunits were identified and designated Cav3.1 (α1G), Cav3.2 (a1H), and Cav3.3 (a1I).
Among the above-noted calcium channels, the T-type calcium channel is known to have many functional aspects which are well defined in various printed publications. The functions of T-type calcium channel include and extend to, for instance, controlling the firing bursts of a nerve cell (See, Huguenard, J. R. et al., Annu. Rev. Physiol. 58, 329–348, 1996), pace maker activity of the heart (See, Zhou, Z & Lipsius, S. L. J. Mol. Cell. Cardiol. 26, 1211–1219, 1994), a hormone aldosterone secretion (See, Rossier, M. F. et al., Endocrinology 137, 4817–4826, 1996) and fertilization (See, Arnoult, C. et al., Proc. Natl. Acad. Sci. 93, 13004–13009, 1996).
T-type calcium channel that is quickly activated and inactivated due to a unique low conductivity typically becomes activated between the range of −40 to −30 mV. However, it is very crucial to maintain the cell membrane voltage prior to activation as it may lead to an undesired effect of rapid inactivation. Because the membrane voltage of most cells expressing the T-type calcium channel is not hyperpolarized sufficiently for activating the same, no methods for studying the membrane voltage currently exist with the exception of an electrophysiological method.
Therefore, studies on signaling pathway mechanism of T-type calcium channel in the nerve cell and scientific researches for developing T-type calcium channel inhibitors are severely undermined. In this respect, it is technically unfeasible, if not impossible, to study and research the T-type calcium channels without resorting to the traditional electrophysiological method. As such, new and innovative methods are needed to improve and enhance the study of the T-type calcium channels.